Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

C-terminus of Hsp70 Interacting Protein (CHIP) and Neurodegeneration: Lessons from the Bench and Bedside.

Current neuropharmacology - 1 Jan 2021

Mylvaganam Sivakami, Earnshaw Rebecca, Heymann Gregory, Kalia Suneil K, Kalia Lorraine V

Abstract excerpt

Neurodegenerative diseases are characterized by the increasing dysfunction and death of neurons, resulting in progressive impairment of a person's mobility and/or cognition. Protein misfolding and aggregation are commonly hypothesized to cause neurotoxicity and, eventually, neuronal degeneration that are associated with these diseases. Emerging experimental evidence, as well as recent findings from human studies,...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cerebellar Ataxia
Share to Huntington Disease

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mutation

Share to Spinocerebellar Ataxias

Share to Ubiquitin-Protein Ligases

Source

Open in PubMed Open full text

Identifiers

PMID: 33200713
DOI: 10.2174/1570159X18666201116145507
PMCID: PMC8686314

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

C-terminus of Hsp70 Interacting Protein (CHIP) and Neurodegeneration: Lessons from the Bench and Bedside.PMID 33200713Read ↗

Ataxia and hypogonadism caused by the loss of ubiquitin ligase activity of the U box protein CHIP.Semantic proximity Read ↗

Clinical and Functional Characterization of a Novel STUB1 Mutation in a Chinese Spinocerebellar Ataxia 48 PedigreeSemantic proximity Read ↗

The molecular basis of spinocerebellar ataxia type 48 caused by a de novo mutation in the ubiquitin ligase CHIP.Semantic proximity Read ↗

Disease-associated mutations in C-terminus of HSP70 interacting protein (CHIP) impair its ability to negatively regulate mitophagy.Semantic proximity Read ↗

Domain-specific decoupling of co-chaperone and ligase functions in <i>STUB1</i> underlies biochemical and clinical heterogeneity in SCA48Semantic proximity Read ↗

STUB1/CHIP mutations cause Gordon Holmes syndrome as part of a widespread multisystemic neurodegeneration: evidence from four novel mutations.Semantic proximity Read ↗

STUB1/CHIP: New insights in cancer and immunitySemantic proximity Read ↗

Phenotype and frequency of STUB1 mutations: next-generation screenings in Caucasian ataxia and spastic paraplegia cohorts.Semantic proximity Read ↗

CHIP suppresses polyglutamine aggregation and toxicity in vitro and in vivo.Semantic proximity Read ↗

U‐box protein carboxyl terminus of Hsc70‐interacting protein (CHIP) mediates poly‐ubiquitylation preferentially on four‐repeat Tau and is involved in neurodegeneration of tauopathySemantic proximity Read ↗

In vitro characterization of six STUB1 variants in spinocerebellar ataxia 16 reveals altered structural properties for the encoded CHIP proteins.Semantic proximity Read ↗

CHIP mutations affect the heat shock response differently in human fibroblasts and iPSC-derived neurons.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.